Supplemental Reading

Small PM and Fujiwara PI. Medical progress:

Management of tuberculosis in the United States. N Engl J Med 2001;345:189-200.

Targeted tuberculin testing and treatment of latent infection. Centers For Disease Control and Prevention MMWR 2000;49:1-54.

Updated Guidelines for the Use of Rifabutin or Rifampin for the Treatment and Prevention of Tuberculosis Among HIV-infected Patients Taking Protease Inhibitors or Non-nucleoside Reverse Transcriptase Inhibitors. Centers For Disease Control and Prevention MMWR 2000;49:185.

Update: fatal and severe liver injuries associated with rifampin and pyrazinamide for latent tuberculosis infection. MMWR 2001;50:733-735.

WHO Expert Committee on Leprosy. World Health Organ Tech Rep Ser 1998,874:1-43.

Answer: B. Rifampin (A) is known to induce certain cytochrome P-450 enzymes and accelerates the metabolism of coadministered drugs that undergo biotransformation through CYP-450. No genetic predetermination is involved in this process. Isoniazid (B) is acetylated to acetyl isoniazid by N-acetyltransferase present in the liver. The human population shows heterogenicity with regard to the rate of acetylation. Rapid acetylators have higher ratios of acetyl isoniazid to isoniazid than do slow acetylators. This genetic determination is rarely important clinically. Pyrazinamide (C) is deaminated by the microsomal drug metabolizing enzyme pyrazinamide deaminase to form pyrazinoic acid. There is no genetic predetermination for this process. Ethambutol (D) is a synthetic antitubercular agent. Orally it is well absorbed and distributed, and about 15% is excreted in the form of two metabolites. This process is not genetically predetermined.

Case Study Genetic Influences on Metabolism

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